Relevant bibliographies by topics / Global cerebral ischaemia

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Academic literature on the topic 'Global cerebral ischaemia'

Author: Grafiati
Published: 4 June 2021
Last updated: 3 February 2022

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Journal articles on the topic "Global cerebral ischaemia"

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Kolvenbach, R., C. Figge, E. Godehardt, and W. Sandmann. "Adenosine agonists and global cerebral ischaemia [letter]." British Journal of Clinical Pharmacology 36, no. 2 (August 1993): 134–35. http://dx.doi.org/10.1111/j.1365-2125.1993.tb04210.x.

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Picozzi, Piero, Nicholas V. Todd, and H. Alan Crockard. "Regional Blood-Brain Barrier Permeability Changes after Restoration of Blood Flow in Postischemic Gerbil Brains: A Quantitative Study." Journal of Cerebral Blood Flow & Metabolism 5, no. 1 (March 1985): 10–16. http://dx.doi.org/10.1038/jcbfm.1985.2.

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A quantitative technique utilising [14C]α-aminoisobutyric acid as a tracer was used to study cerebrovascular permeability in 22 Mongolian gerbils. Seven other animals were used to measure cerebral blood volumes. Global cerebral ischaemia was produced by temporary bilateral carotid artery occlusion (60 min) in 16 gerbils that were sacrificed at 1, 2, and 3 h following reperfusion. The blood-to-brain transfer constant was significantly increased after 2 h of reperfusion in the ischaemic zones and also in structures, like the cerebellum, not supplied by the carotid artery and not ischaemic during the vessel occlusion. The blood-brain barrier (BBB) alterations were coincident with the onset of ischaemia—induced seizures that were accompanied by sudden “spikes” of systemic blood pressure. Epilepsy may play an important role in the development of BBB damage in this ischaemic model, and this factor must be considered in the interpretation of BBB damage data in gerbils.
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Spencer, Sarah J., Roland N. Auer, and Quentin J. Pittman. "Rat Neonatal Immune Challenge Alters Adult Responses to Cerebral Ischaemia." Journal of Cerebral Blood Flow & Metabolism 26, no. 4 (August 10, 2005): 456–67. http://dx.doi.org/10.1038/sj.jcbfm.9600206.

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Infection, inflammation, and hyperthermia associated with cerebral ischaemia are known to contribute to enhanced neuronal cell loss and more severe behavioural deficits. Because neonatal exposure to an immune challenge has been shown to alter the severity of inflammatory and febrile responses to a further immune challenge experienced in adulthood, we hypothesised that this could also alter temperature responses and neuronal survival after ischaemia. Thus, male Sprague–Dawley rats were treated at postnatal day 14 with a single injection of the bacterial endotoxin lipopolysaccharide (LPS) and were examined as adults for temperature changes, behavioural deficits, and neuronal cell loss associated with global cerebral ischaemia after a two-vessel occlusion (2 VO). Neonatally LPS-treated rats showed behavioural differences in a novel object exploration paradigm, as well as altered temperature responses to the 2 VO compared with neonatally salinetreated controls. Interestingly, these neonatally LPS-treated rats also showed increased cell loss in the central nucleus of the amygdala, a region that is important in the processing of emotional responses, but that is not usually examined in animal models of cerebral ischaemia. No differences were seen in the CA1, CA3, or dentate gyrus regions of the hippocampus. This work shows the importance of examining brain regions other than the hippocampus in association with global ischaemia. We also highlight the importance of the early period of development in programming an animal's ability to deal with injury such as cerebral ischaemia in adulthood.
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O'Neill, Michael J., Caroline A. Hicks, Mark A. Ward, Geraldine P. Cardwell, Jean-Michel Reymann, Hervé Allain, and Daniele Bentué-Ferrer. "Dopamine D2 receptor agonists protect against ischaemia-induced hippocampal neurodegeneration in global cerebral ischaemia." European Journal of Pharmacology 352, no. 1 (July 1998): 37–46. http://dx.doi.org/10.1016/s0014-2999(98)00333-1.

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Abels, C., F. Röhrich, S. Corvin, R. Meyermann, A. Baethmann, and L. Schürer. "Leukocyte-Endothelium-Interaction in Pial Vessels Following Global, Cerebral Ischaemia." Acta Neurochirurgica 142, no. 3 (March 15, 2000): 333–39. http://dx.doi.org/10.1007/s007010050043.

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Hodges, Helen, Alan Nelson, David Virley, Timothy R. Kershaw, and John D. Sinden. "Cognitive Deficits Induced by Global Cerebral Ischaemia: Prospects for Transplant Therapy." Pharmacology Biochemistry and Behavior 56, no. 4 (April 1997): 763–80. http://dx.doi.org/10.1016/s0091-3057(96)00424-8.

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Kil, H. Y., W. Sl Oh, and T. H. Han. "Fentanyl alters cytokine level during global cerebral ischaemia/reperfusion in rats." European Journal of Anaesthesiology 17, Supplement 19 (2000): 90. http://dx.doi.org/10.1097/00003643-200000002-00291.

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Davidson, Joanne O., Caroline A. Yuill, Guido Wassink, Laura Bennet, and Alistair J. Gunn. "Spontaneous Pre-Existing Hypoxia Does Not Affect Brain Damage after Global Cerebral Ischaemia in Late-Gestation Fetal Sheep." Developmental Neuroscience 37, no. 1 (November 14, 2014): 56–65. http://dx.doi.org/10.1159/000368306.

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There is considerable evidence that a mild, non-injurious insult can protect (precondition) against a subsequent injurious insult. Typically, protection is seen when the gap between insults is several days to a week. However, the effect of mild but persistent hypoxia is unknown. In this study we examined the hypothesis that mild pre-existing hypoxia (PaO2 <17 mm Hg) would reduce neural injury in chronically instrumented late-gestation (0.85 gestation) fetal sheep exposed to 30 min of global cerebral ischaemia induced by bilateral carotid artery occlusion (normoxia: n = 9 vs. pre-existing hypoxia: n = 9) or normoxia plus sham ischaemia (sham controls: n = 9). Histopathology was assessed after 7 days of recovery. Fetuses with pre-existing hypoxia had lower PaO2 values (16.1 ± 0.6 vs. 26.0 ± 1.1 mm Hg) and were lighter at post-mortem (4,033 ± 412 vs. 5,261 ± 238 g) compared to normoxic fetuses. Cerebral ischaemia was associated with secondary cortical oedema and seizures, reduced final EEG power, loss of sleep state cycling, and significant loss of neurons and oligodendrocytes, with no significant effect of pre-existing hypoxia. Pre-existing hypoxia was associated with a significantly attenuated rise in mean arterial pressure between 18 and 36 h and slower resolution of cortical oedema between 96 and 150 h after ischaemia. These data suggest that chronic hypoxia is not associated with a significant preconditioning effect.
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Von Lubitz, Dag K. J. E., R. C. S. Lin, Robert J. McKenzie, Thomas M. Devlin, and R. Tyler McCabe. "A novel treatment of global cerebral ischaemia with a glycine partial agonist." European Journal of Pharmacology 219, no. 1 (August 1992): 153–58. http://dx.doi.org/10.1016/0014-2999(92)90594-t.

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Endo, H., A. Saito, and P. H. Chan. "Mitochondrial translocation of p53 underlies the selective death of hippocampal CA1 neurons after global cerebral ischaemia." Biochemical Society Transactions 34, no. 6 (October 25, 2006): 1283–86. http://dx.doi.org/10.1042/bst0341283.

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p53, a tumour suppressor, is involved in DNA repair and cell death processes and mediates apoptosis in response to death stimuli by transcriptional activation of pro-apoptotic genes and by transcription-independent mechanisms. In the latter process, p53 induces permeabilization of the outer mitochondrial membrane by forming an inhibitory complex with a protective Bcl-2 family protein, resulting in cytochrome c release in several cell line systems. However, it is unclear how the mitochondrial p53 pathway mediates neuronal apoptosis after cerebral ischaemia. We examined interaction between the mitochondrial p53 pathway and vulnerable hippocampal CA1 neurons using a tGCI (transient global cerebral ischaemia) rat model. We showed mitochondrial translocation of p53 and its binding to Bcl-XL. Mitochondrial p53 translocation, interaction between p53 and Bcl-XL, and cytochrome c release from mitochondria and subsequent CA1 neuronal death were prevented by pifithrin-α, a p53-specific inhibitor. These results suggest that the mitochondrial p53 pathway plays a role in delayed CA1 neuronal death after tGCI.
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Dissertations / Theses on the topic "Global cerebral ischaemia"

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Whitfield, Peter Cyril. "Gene expression after global and focal cerebral ischaemia." Thesis, University of Southampton, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242632.

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Gregory, Lloyd James. "Monitoring the neuropathogenic processes following global cerebral ischaemia using magnetic resonance imaging." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325067.

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Jeffs, Graham J. "The effect of sodium/calcium exchanger 3 (NCX3) knockout on neuronal survival following global cerebral ischaemia in mice." University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2007. http://theses.library.uwa.edu.au/adt-WU2008.0063.

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Cerebral ischaemia is a leading cause of disability and death world-wide. The only effective treatments are thrombolytic therapy (plasminogen activator; tPA) and hypothermia (33?C). However, tPA has limited clinical application due to its short therapeutic time window and its specific application in thrombo-embolic stroke. Moderate hypothermia (33?C) is only being used following cardiac arrest in comatose survivors. Hence more treatments are urgently required. The first step in developing new treatments is the identification and characterisation of a potential therapeutic target. Since brain damage following cerebral ischaemia is associated with disturbances in intracellular calcium homeostasis, the sodium-calcium exchanger (NCX) is a potential therapeutic target due to its ability to regulate intracellular calcium. Currently, however there is uncertainty as to whether the plasma membrane NCX has a neuroprotective or neurodamaging role following cerebral ischemia. To address this issue I compared hippocampal neuronal injury in NCX3 knockout mice (Ncx3-/-) and wild-type mice (Ncx3+/+) following global cerebral ischaemia. In order to perform this study I first established a bilateral common carotid occlusion (BCCAO) model of global ischaemia in wild-type C57/BlHsnD mice using controlled ventilation. After trials of several ischaemic time points, 17 minutes was established as the optimum duration of ischaemia to produce selective hippocampal CA1 neuronal loss in the wild-type mice. I then subjected NCX3 knockout and wild-type mice to 17 minutes of ischaemia. Following the 17 minute period of ischaemia, wild-type mice exhibited 80% CA1 neuronal loss and 40% CA2 neuronal loss. In contrast, NCX3 knockout mice displayed > 95% CA1 neuronal loss and 95% CA2 neuronal loss. Following experiments using a 17 minute duration of global ischaemia, a 15 minute duration of ischaemia was also evaluated. Wild-type mice exposed to a 15 minute period of ischaemia, did not exhibit any significant hippocampal neuronal loss. In contrast, NCX3 knockout mice displayed 45% CA1 neuronal loss and 25% CA2 neuronal loss. The results clearly demonstrate that mice deficient for the NCX3 protein are more susceptible to global cerebral ischaemia than wild-type mice. My findings showing a neuroprotective role for NCX3 following ischaemia, suggest that the exchanger has a positive role in maintaining neuronal intracellular calcium homeostasis. When this function is disrupted, neurons are more susceptible to calcium deregulation, with resultant cell death via calcium mediated pathways. Therefore, improving NCX activity following cerebral ischaemia may provide a therapeutic strategy to reduce neuronal death.
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Nelson, Alan John. "Cognitive deficit by global cerebral ischaemia in the rat : strategies to promote functional recovery by drug treatment and neural transplantation." Thesis, King's College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265185.

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Books on the topic "Global cerebral ischaemia"

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Gaddam, Samson Sujit Kumar, and Claudia S. Robertson. Cerebral blood flow and perfusion monitoring in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0222.

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Prevention of secondary cerebral ischaemic insults is an important management strategy in acute neurological conditions. Monitoring of cerebral perfusion may aid in early identification of ischaemic insults and help with management. A number of tools are available for this purpose. Cerebral perfusion pressure (CPP) is the simplest assessment of cerebral perfusion, but in some cases ischaemia can be present even with a normal CPP. Cerebral blood flow (CBF) imaging, either with computed tomography or magnetic resonance imaging techniques, can provide quantitative regional CBF measurement, but only at a single instance in time. Such studies are valuable in the diagnosis of ischaemia, but are difficult for the management of critically-ill patients. CBF can also be measured within the intensive care unit (ICU), either directly or indirectly through the measurement of cerebral oxygenation. These monitors provide a more continuous measure of CBF, and are more useful in assessing response to treatment. Some of the ICU tools monitor global perfusion and some assess perfusion only in a local area of brain surrounding the monitor. With local monitors, the location of the probe is important for interpretation of the findings.
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De Deyne, Cathy, Ward Eertmans, and Jo Dens. Neurological assessment of the acute cardiac care patient. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0016_update_001.

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Many techniques are currently available for cerebral physiological monitoring in the intensive cardiac care unit environment. The ultimate goal of cerebral monitoring applied during the acute care of any patient with/or at risk of a neurological insult is the early detection of regional or global hypoxic/ischaemic cerebral insults. In the most ideal situation, cerebral monitoring should enable the detection of any deterioration before irreversible brain damage occurs or should at least enable the preservation of current brain function (such as in comatose patients after cardiac arrest). Most of the information that affects bedside care of patients with acute neurologic disturbances is now derived from clinical examination and from knowledge of the pathophysiological changes in cerebral perfusion, cerebral oxygenation, and cerebral function. Online monitoring of these changes can be realized by many non-invasive techniques, without neglecting clinical examination and basic physiological variables—with possible impact on optimal cerebral perfusion/oxygenation—such as invasive arterial blood pressure monitoring or arterial blood gas analysis.
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De Deyne, Cathy, and Jo Dens. Neurological assessment of the acute cardiac care patient. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0016.

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Many techniques are currently available for cerebral physiological monitoring in the intensive cardiac care unit environment. The ultimate goal of cerebral monitoring applied during the acute care of any patient with/or at risk of a neurological insult is the early detection of regional or global hypoxic/ischaemic cerebral insults. In the most ideal situation, cerebral monitoring should enable the detection of any deterioration before irreversible brain damage occurs or should at least enable the preservation of current brain function (such as in comatose patients after cardiac arrest). Most of the information that affects bedside care of patients with acute neurologic disturbances is now derived from clinical examination and from knowledge of the pathophysiological changes in cerebral perfusion, cerebral oxygenation, and cerebral function. Online monitoring of these changes can be realized by many non-invasive techniques, without neglecting clinical examination and basic physiological variables such as invasive arterial blood pressure monitoring or arterial blood gas analysis.
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Haunton, Victoria, Aung Sett, Amit Mistri, and Martin Fotherby. Stroke. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0227.

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The World Health Organization defines stroke as ‘a clinical syndrome consisting of rapidly developing clinical signs of focal (at times global) disturbance of cerebral function lasting greater than 24 hours (or leading to death) with no apparent cause other than that of vascular origin’. Transient ischaemic attack (TIA) is defined as a rapid presentation of neurological deficit with complete recovery within 24 hours of the onset of symptoms. However, the 24-hour cut-off is arbitrary, has no biological basis, and is of limited use clinically. A shorter duration is now regarded as more appropriate, although it has yet to be universally accepted. In clinical practice, stroke and TIA are best thought of as comprising a continuum, as they have similar pathological mechanisms, etiologies, and management strategies. While subarachnoid haemorrhage is a type of stroke based on the above definition, it is not covered in this chapter, as its pathophysiology, clinical manifestations, and management are distinct from those for ischaemic stroke and haemorrhagic stroke.
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Book chapters on the topic "Global cerebral ischaemia"

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Rossi, Sandra, M. Balestreri, D. Spagnoli, G. Bellinzona, V. Valeriani, P. Bruzzone, M. Maestri, and N. Stocchetti. "Oxygen Delivery and Oxygen Tension in Cerebral Tissue During Global Cerebral Ischaemia: A Swine Model." In Brain Edema XI, 199–202. Vienna: Springer Vienna, 2000. http://dx.doi.org/10.1007/978-3-7091-6346-7_40.

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